Background: Recent evidences suggest that hypogonadism is an important risk factor
for lower urinary tract symptoms and benign prostatic hyperplasia. Several papers have discussed
the role of chronic inflammation in the development of BPH, which may be modulated by the hypogonadal
state. Soluble Urokinase-type Plasminogen Activator Receptor (suPAR), known protein
marker of systemic inflammation, can be assayed in the seminal plasma and represents a reliable
and sensitive marker of inflammation for the Male Accessory Gland Inflammation (MAGI).
Objective: The aim of this study has been to investigate if seminal suPAR is elevated in MAGI with
hypogonadism and if suPAR represent a useful marker of abacterial inflammation in hypogonadism.
Methods: We included in the study twenty male patients aged between 25 and 55 year-old with
secondary postsurgical hypogonadism. The same patients were also evaluated after a 3-month of
Testosterone Replacement Therapy (TRT), to evaluate the effect of androgen replacement therapy
on suPAR. Ten fertile men have been enrolled as a control group in the protocol. SuPAR concentrations
were assayed on seminal plasma using an Enzyme-Linked Immunosorbent Assay (ELISA)
Results: Hypogonadic patients presented significantly increased levels of seminal suPAR respect to
controls (86.1±36.8 vs 55.2±20.0 ng/mL, p<0.05). TRT in hypogonadic patients has been associated
with a significant reduction of suPAR levels as reported in the control group (50.9±22.91 vs
86.1±36.8 ng/ml p<0.05).
Conclusions: These results confirm the role of suPAR as a protein marker of MAGI and support
the hypothesis that hypogonadism induces a state of inflammation in male accessory glands which
is involved in male infertility. Moreover demonstrated that testosterone treatment probably exerts a
positive effect on MAGI and infertility as documented by reduction of suPAR levels in hypogonadic